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. Author manuscript; available in PMC: 2016 May 1.
Published in final edited form as: Trends Neurosci. 2015 Apr 14;38(5):279–294. doi: 10.1016/j.tins.2015.03.003

Figure 2. Stress-induced internalization of AMPARs and NMDARs in the prefrontal cortex is mediated by ubiquitination and proteosomal degradation.

Figure 2

AMPAR-mediated (A, −70 mV, representative currents at right) and NMDAR-mediated (B, +60 mV) excitatory currents recorded from layer V pyramidal cells in response to a range of stimulation intensities in slices from unstressed control rats (open circle) and rats subjected to chronic restraint stress (filled triangle) or chronic unpredictable stress (filled square). Stress depressed both components regardless of stimulation intensity. C. Chronic restraint stress decreased both expression and plasma membrane surface insertion of GluA1 and GluN1 receptor subunits. D. Pharmacological inhibition of proteosomal degradation prevented decreases in AMPAR-mediated synaptic currents in response to chronic stress, but had no effect in unstressed animals. Representative currents shown at right. Modified with permission from Yuen et al., 2012 [49].